Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 Nov 1;50(11):1104-1113.
doi: 10.1093/abbs/gmy109.

miR-23b promotes cutaneous wound healing through inhibition of the inflammatory responses by targeting ASK1

Hongzhi Li  1   2   3 , Xiao Han  4 , Kuiyang Zuo  3 , Li Li  3 , Jieting Liu  3 , Xiaohuan Yuan  3 , Yongchao Shen  3 , Minglong Shao  5 , Daxin Pang  1 , Yanhui Chu  3 , Binghai Zhao  2   3
Affiliations
Free article

miR-23b promotes cutaneous wound healing through inhibition of the inflammatory responses by targeting ASK1

Hongzhi Li et al. Acta Biochim Biophys Sin (Shanghai). .
Free article

Abstract

Wound healing is a complicated event that develops in three overlapping phases: inflammatory, proliferative, and remodeling. MicroRNAs (miRNAs) have been proved to play an important role in the healing process of skin trauma, and alteration of specific miRNA expression during different phases may be associated with abnormal wound healing. In this study, we determined the variation of miR-23b expression after trauma in normal mice and in cultured cells exposed to lipopolysaccharide. We further demonstrated that excessive miR-23b could significantly accelerate wound healing in vivo. Up-regulation of miR-23b decreases infiltration of inflammatory cells, as evidenced by pathologic staining. Meanwhile, miR-23b could significantly inhibit the expression of pro-inflammatory cytokines, including TNF-α, IL-1β, IL-6, and Ccl2, and significantly increase anti-inflammatory factor IL-10. Furthermore, miR-23b could also promote α-SMA expression in a fiber pattern and increase the expression of Col1a1 and Col3a1. Importantly, we also showed that miR-23b could inhibit inflammation to promote wound healing by targeting apoptotic signal-regulating kinase 1 (ASK1). Notably, knockdown of ASK1 could reduce inflammation factor expression in vitro. Together, our data reveal that miR-23b is a potent therapeutic agent for cutaneous wound healing that shortens the period of inflammatory responses and promotes keratinocyte migration for the re-epithelialization of wound sites.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles